Follow-up studies on individuals who suffer severe head injury give a picture of poor cognitive and psychosocial outcome. However, recent evidence suggests that with the passage of time, many individuals make adjustments that compensate for early disability, leading to a reduction in social handicap with a corresponding improvement in life quality and personal satisfaction. This article will attempt to briefly review the main sources of evidence contributing to long-term outcome following serious head trauma.

In the long term after traumatic brain injury, the most disabling problems are generally related to neuropsychiatric sequelae, including personality change and cognitive impairment, rather than neurophysical sequelae. Cognitive impairment after severe injury is likely to include impaired speed of information processing, poor memory and executive problems. Personality change may include poor motivation, and a tendency to be self-centred and less aware of the needs of others. Patients may be described as lazy and thoughtless. Some become disinhibited and rude. Agitation and aggression can be very difficult to manage. Anxiety and depression symptoms are quite frequent and play a role in the development of persistent post-concussion syndrome after milder injury. Depression may be associated with a deterioration in disability over time after injury. Psychosis is not unusual though it has been difficult to confirm that traumatic brain injury is a cause of schizophrenia. Head injury may, many years later, increase the risk of Alzheimer’s disease. Good rehabilitation probably minimizes the risk of psychiatric sequelae, but specific psychological and pharmacological treatments may be needed.

Neurobehavioural sequelae of traumatic brain injuries require an appropriate/effective pharmacological response in that they represent an important cause of disability. In this field, there is no evidence that reaches the level of a standard: there are guidelines on the use of methylphenidate, donepezil and bromocriptine for the treatment of cognitive disturbances, for the non-use of phenytoin and for the use of β-blockers for controlling aggressiveness. Resolving a single symptom is not relevant in a rehabilitation project if it is not in the context of a more complex picture of neurobehavioural recovery, in which the positive and negative effects of every therapeutic choice are considered. For example, phenytoin could be used for the positive control of epileptic crises but is not advised since it impedes the recovery of cognitive functions in general. Analogous effects not yet identified may concern benzodiazepine, neuroleptics and other sedatives usually prescribed in cases of cranial trauma. Psychotropic drugs are considered to be able to influence the neuronal plasticity processes. Studies on animals have shown that the administration of D-amphetamine combined with sensorial-motor exercise produces the steady acceleration of motor recovery, which acts as a catalyst to the neurological recovery process. On the other hand, α1-NA receptor antagonist drugs produce negative effects; these include clonidine (antihypertension) and haloperidol (neuroleptic). Studies need to be carried out to evaluate the effectiveness of particular drugs. These studies need to focus not only on the disappearance of symptoms but also on the positive and negative effects on overall rehabilitation and on the neurobiological recovery of the patient.

The pathophysiology of hydrocephalus can be modelled and described in terms of altered biomechanical parameters. Shunting is aimed to correct the patient’s cerebrospinal fluid dynamics, compensating for inadequate cerebrospinal fluid re-absorption or insufficient volume buffering reserve. Computerized infusion studies implement intracranial pressure and arterial pressure signal processing and model analysis to allow the estimation of cerebrospinal dynamics variables such as cerebrospinal fluid outflow resistance, brain compliance and pressure–volume index, estimated sagittal sinus pressure, cerebrospinal fluid formation rate, compensatory reserve and cerebral vasoreactivity.

Infusion studies can assist in the prognostication of normal pressure hydrocephalus and in the diagnosis of idiopathic intracranial hypertension. The technique is also helpful in the assessment of shunt malfunction, including posture-related over-drainage and shunt obstruction.

Since shunting is almost a purely mechanical treatment that radically affects pressure–volume compensation, patients’ cerebrospinal fluid hydrodynamics compensation should be examined before a shunt is implanted. Apart from an opening pressure and a resistance to cerebrospinal fluid outflow, pulse amplitude of intracranial pressure and the content of vasogenic waves are useful to gauge cerebrospinal fluid dynamics. Infusion studies, although invasive, may help with the decision about surgery. They also provide basic information for further management of shunted patients, when complications, such as shunt blockage, under- and over-drainage, arise.

Sepsis, a systemic inflammatory response to infection, is a leading cause of death in intensive care units. Recent investigations into the pathogenesis of sepsis reveal a biphasic inflammatory process. An early phase is characterized by pro-inflammatory cytokines (e.g. tumour necrosis factor-α), whereas a late phase is mediated by an inflammatory high-mobility group box 1 and an anti-inflammatory interleukin-10. Inflammation aberrantly activates coagulation cascades as sepsis progresses. This dual inflammatory response concomitant with dysregulated coagulation partially accounts for unsuccessful anti-cytokine therapies that have solely targeted early pro-inflammatory mediators (e.g. tumour necrosis factor-α). In contrast, activated protein C, which modifies both inflammatory and coagulatory pathways, has improved survival in patients in severe sepsis. Inhibition of the late mediator high-mobility group box 1 improves survival in established sepsis in pre-clinical studies. In addition, recent advances in molecular medicine have shed light on two novel experimental interventions against sepsis. Accelerated apoptosis of lymphocytes has been shown to play an important role in organ dysfunction in sepsis and techniques to suppress apoptosis have improved survival rate in sepsis models. The vagus nerve system has also been shown to suppress innate immune response through endogenous release and exogenous administration of cholinergic agonists, ameliorating inflammation and lethality in sepsis models.

Activation of inflammation is the hallmark of pathological processes that follow acute injury. This process is mediated by inflammatory cytokines and adhesion molecules that reside on the surface of endothelium, leucocyte and inflammatory cells. Attenuation of the adhesion cascade has been the subject of several basic science and clinical trials in the management of neurological injury. This review will highlight the role of adhesion molecules in the evolution of secondary injury after cerebral ischaemia and trauma. Potential therapeutic avenues will then be discussed.

It is widely acknowledged that the quality of research is greatly improved when nurses are involved at the investigators’ site. Many papers highlight the knowledge, skills and expertise required by nurses for the conduct of trials. The known skills include reliability, organization, communication, motivation, self-discipline and critical thought. The responsibilities of nurses in the conduction of research trials are wide ranging from the collection and recording of data, recruitment and screening of patients, ensuring informed consent has been gained, randomization of drugs, the follow-up of patients to development and training for staff to the required international standards. In the past, clinical research nurses have been considered as data collectors by their peers, due to the lack of knowledge of the true extent of the role of the clinical research nurse. The rise in popularity of the role and the publication of an employment brief for clinical research nurses by the Royal College of Nursing (RCN) and the UK Clinical Research Collaboration (UKCRC) publication on ‘Developing the best research professionals’ has readdressed this prior imbalance; recognizing in detail their role, knowledge, skills, expertize with appropriate grading and remuneration. The role of the clinical research nurse in the neuroscience setting is equally as diverse with the added requirement of a higher level of knowledge and understanding of the pathophysiology of neurological diseases and specific skills required to work in the intensive care environment. This paper will attempt to explore the role of the specialized neurosciences intensive care nurse and the relationship with high-quality neuroscience research.

Nurses have become independent over the last few decades in Italy, thanks to a series of legislative changes. When dealing with organ donation, the nurses usually face unexpected and complex situations from both a technical and interpersonal point of view. When the death of a loved one has to be communicated to the family, the coordinator nurse, along with the doctor, talks with the relatives to help them decide whether or not to donate organs. It is fundamental that the death of the patient is communicated by the doctor in charge of the case and this has to be done before the question of donation is raised. The idea of donation is suggested when we believe the family has understood that their beloved is dead. We try to adapt our communication style to the background of the family. Experience has shown us that these situations are emotionally complex and tiring for both the family members and health workers. Sometimes the stress level amongst health workers is so high that psychological support is needed after the interview. If the family decides to donate, the restitution phase is very important. A meeting is organized for a month after the event to inform the relatives of the success of donation.

Transcranial Doppler is an innovative, flexible, accessible tool for the bedside monitoring of static and dynamic cerebral flow and treatment response. Introduced by Rune Aaslid in 1982, it has become indispensable in clinical practice. The main obstacle to ultrasound penetration of the skull is bone. Low frequencies, 1–2 MHz, reduce the attenuation of the ultrasound wave caused by bone. Transcranial Doppler also provides the advantage of acoustic windows representing specific points of the skull where the bone is thin enough to allow ultrasounds to penetrate. There are four acoustic windows: transtemporal, transorbital, suboccipital and retromandibular. The identification of each intracranial vessel is based on the following elements: (a) velocity and direction; (b) depth of signal capture; (c) possibility of following the vessel its whole length; (d) spatial relationship with other vessels; and (e) response to homolateral and contralateral carotid compression. The main fields of clinical application of transcranial Doppler are assessment of vasospasm, detection of stenosis of the intracranial arteries, evaluation of cerebrovascular autoregulation, non-invasive estimation of intracranial pressure, measure of effective downstream pressure and assessment of brain death. Mean flow velocity is directly proportional to flow and inversely proportional to the section of the vessel. Any circumstance that leads to a variation of one of these factors can thus affect mean velocity. The main pathological condition affecting flow velocity is the vasospasm. Vasospasm is a frequent complication of subarachnoid haemorrhage, it often remains clinically silent and the factors that make it symptomatic are largely unknown. Threshold velocities above which vasospasm comes into place are well defined as regards the median cerebral artery, while there is no consensus for the other vessels. Nevertheless, an increase in velocity alone is not sufficient to arrive at a diagnosis of vasospasm; a condition of hyperaemia also presents with an increase in flow velocity. The Lindegaard Index has therefore been introduced, which is defined by the ratio between the mean flow velocity in the median cerebral artery and the mean flow velocity in the internal carotid artery. Criteria for diagnosis of a stenosis >50% of an intracranial vessel with transcranial Doppler include: (a) segmentary acceleration of flow velocity; (b) drop in velocity below the stenotic segment; (c) asymmetry; and (d) circumscribed flow disturbances (turbulence and musical murmur). The transcranial Doppler enables us to assess both components of self-regulation. The static component is measured by observing changes in flow velocity caused by pharmacologically induced episodes of hypertension and hypotension. The dynamic component of autoregulation can be measured using a method devised by Aaslid known as the ‘cuff test’. A very effective and safe device for measuring cerebral autoregulation is the transient hyperaemic response test. This test is based on the compensatory vasodilatation of the arterioles, which occurs after brief compression of the common carotid. Csonyka proposed the following formula based on clinical observation for the calculation of cerebral perfusion pressure: CPP = MAP × FVd/FVm + 14. Brain death is defined as the irreversible cessation of all functions of the whole brain. The clinical criteria are usually considered sufficient to establish a diagnosis of brain death; however, they might not be sufficient in patients who have been on sedatives or when there are ethical or legal controversies. Many authors have demonstrated the existence of a transcranial Doppler pattern, which is typical of brain death.

Neuromuscular complications encountered in intensive care can be due to peripheral nerves (polyneuropathies), muscles (myopathies), neuromuscular end-plate (transmission deficit) or a combination of these. Neurophysiopathological tests that enable us to diagnose and maybe differentiate between these causes are essentially electroneurographs and electromyographs. These assess, either directly or indirectly, the integrity of the peripheral system, both sensory (centripetal afferent pathways) and motor (lower motor neurones, neuromuscular junction, muscle membrane and contractile substrate). Electrical activity in the muscle is measured using a special device (an electromyograph) comprising preamplifiers, a computer with special programmes and algorithms for analysing, digitalizing, amplifying and filtering the recorded signal and a monitor on which to visualize the on-line trace. The machine also has speakers. These serve to recognize and identify the physiological events being recorded as they make such unusual, individual sounds. An electric stimulator with constant current can be used to stimulate branches of superficial nerves (motor, sensory or mixed) so that electric conduction speed can be studied and the sensory or motor response analysed. The results can be saved on a hard disc or on any magnetic or digital support, viewed off-line or even printed.